Figure 3From: Adjusting the compass: new insights into the role of angiogenesis in Alzheimer’s diseaseSchematic model of how angiogenesis results in the breakdown of the blood–brain barrier (BBB) in Alzheimer’s disease (AD). Impaired cerebral blood flow (CBF) [4–8, 23, 25–28], tight junction (TJ) disruption [21, 22, 67], and disturbances in proteins regulating amyloid beta (Aβ) levels in the brain, such as receptor for advanced glycation products (RAGE) and lipoprotein receptor-related protein 1 (LRP1) [31–38], are factors contributing to elevated Aβ levels and subsequent angiogenesis [24, 48, 61, 67, 70]. Inflammation gives rise to elevated pro-angiogenic cytokines such as vascular endothelial growth factor (VEGF), further promoting vascular remodeling in the AD brain [47, 51–54]. Angiogenesis may also occur as a compensatory response to impaired CBF [47]. These processes lead to further Aβ secretion by endothelial cells, exacerbating angiogenesis and the production of reactive oxygen species (ROS), endothelial damage, and neurotoxicity.Back to article page